1. Field of the Invention:
The present invention relates to an oral composition to effectively prevent and remedy dentinal hypersensitivity.
2. Description of the Prior Art:
Dentinal hypersensitivity is a name of disease given after the clinical symptoms. It causes acute transient pain when the dentin receives thermal, chemical, mechanical, physicochemical, electrical, and other external stimuli, because the dentin is exposed due to the loss of enamel or cement which results from dental caries, attrition, abrasion, or recession of gingiva. The pain is induced when the patient eats a sweet food or sour fruit, or drinks cold water, or brushes his teeth. This pain adversely affects one's eating habits and oral hygiene.
The following two theories are main the hypotheses for the transmission mechanism of pain-producing stimulus in dentinal hypersensitivity.
(A) Transducer Theory . . . Odontoblasts or their processes existing in dentinal tubules work as a receptor for stimulus to transmit its information to nerve fibers in the pulp.
(B) Hydrodynamic Theory . . . Stimulus applied to dentinal surface causes the movement of dentinal fluid which then stimulates free nerve endings existing in the dentin-pulp region, thereby causing pain.
At present, the latter theory (hydrodynamic theory) is predominant with the support by M. Branstrom (Calorinsca Institute), Pashley (Georgia Pharmaceutical College), and B. Matthew (Bristol University). A human molar dentin has 20,000 to 30,000 dentinal tubules per mm.sup.2 (about 1.0 .mu.m in diameter) at the enamel side and 30,000 to 40,000 tubules per mm.sup.2 (about 3.0 .mu.m in diameter) at the pulp side. When the enamel or cement is lost, the external stimuli applied to the surface of the exposed dentin cause the fluid flow in the dentinal tubules, thereby exciting the sensory nerve in the dental pulp, and then giving a pain.
The effective means to relieve, eliminate, or prevent the dentinal hypersensitivity is to close or block the orifice of the dentinal tubules, thereby suppressing or inhibiting the transmission of stimuli.
Studies of therapeutic agents for improving dentinal hypersensitivity have been carried out from considerably old times. Grossman, L. E. (1935) listed six ideal prerequisites for the therapeutic agent for this disease.
(1) Non-irritant to the pulp
(2) Relatively painless upon application
(3) Easily applied
(4) Rapid in action
(5) Effective for a long time
(6) without staining effects
It is said that there are no methods meeting all these prerequisites at present.
According to the aforementioned hypotheses for the stimulus transmission mechanism, the currently performed therapeutics are roughly categorized into the following two groups.
(I) The methods of neurophysiologically desensitizing the stimulus-receptors (odontblasts and nerve fibers) by means of medicines.
(II) The methods of inhibiting the transmission of stimulus to free nerve endings by suppressing the movement of dentinal fluid (according to the hydrodynamic theory).
The tangible methods belonging to the category (I) include those in which various kinds of cauteries and medicines having the effect of denaturing and coagulating protein (such as formalin, paraformaldehyde, zinc chloride, strontium chloride, carbonates and silver compounds) are applied. The tangible methods belonging to the category (II) include the methods of occluding tubular orifices (with various kinds of dental cements, adhesive resins and periodontal surgical packs), the methods of constricting dentinal tubules by depositing calcium salts or water-insoluble salts (such as various kinds of fluorides, strontium chloride, citrates, mixture consisting of potassium ferrocyanide and zinc chloride and silver compounds) around tubular orifices, and the methods of constricting dentinal tubules by accelerating the formation of secondary dentin (by means of calcium hydroxide, paraformaldehyde, etc.). These methods of various kinds are applied according to the symptoms of patient suffering dentinal hypersensitivity. However, as seen from the six prerequisites determined by Grossman, all of these methods have various disadvantages and problems which should be improved such as a complicate technique, a possibility of causing damage to oral tissue, a small measure of success and staining effects.
Heretofore, there are proposed several oral compositions intended for the prevention or treatment of dentinal hypersensitivity. However, most of them are not intended for occlusion of tubular orifices; in other words, they are not designed to prevent the nerve from being stimulated by the movement of the dentinal tubule fluid, but are designed for performing indirect prevention and treatment through desensitizing the nerve.
For example, the U.S. Pat. No. 3,514,513 discloses the use of aluminum chlorohydroallantoinate as a therapeutic ingredient for dentinal hypersensitivity. However, aluminum chlorohydroallantoinate is not so effective, as shown in the Examples shown below, when evaluated by using the split chamber device for measuring the dentin hydrauric conductance described by Pashley, D. H. (J. Dent. Res., 60(3)686-698, 1981) which the present inventors accepted to examine the effect on the occlusion of tubular orifices. This method is suitable as an evaluation of the agents having the ability to reduce the dentin permeability.
There is also known an oral composition which contains an aluminum compound and fluorine compound together for the prevention of dental calculus (U.S. Pat. No. 4,146,605). This patent discloses that the composition can be incorporated with citric acid or lactic acid. The composition containing such an acid has the pH value lower than 4.5. The low pH is not effective for the occlusion of tubular orifices, as shown in the experimental examples that follow.
There is disclosed in U.S. Pat. No. 3,651,207 a mouthwash containing aluminum dihydroxyallantoinate, citric acid, tartaric acid, and sodium hydrogenphosphate. This mouthwash is not effective for dentinal hypersensitivity because the content of aluminum is low relative to the content of citric acid and tartaric acid.